ArticleAnti-cancer drugs2008
Protein kinase C beta in malignant pleural mesothelioma.
Article in Anti-cancer drugs, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Expression and activity of eIF6 trigger malignant pleural mesothelioma growth in vivo.Oncotarget · 2015Article
- Role of protein kinase C β and vascular endothelial growth factor receptor in malignant pleural mesothelioma: Therapeutic implications and the usefulness of Caenorhabditis elegans model organism.Journal of carcinogenesis · 2011Article
- EphA2 mutation in lung squamous cell carcinoma promotes increased cell survival, cell invasion, focal adhesions, and mammalian target of rapamycin activation.The Journal of biological chemistry · 2010Article
- MET, HGF, EGFR, and PXN gene copy number in lung cancer using DNA extracts from FFPE archival samples and prognostic significance.Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer · 2009Article
- MET/PKCbeta expression correlate with metastasis and inhibition is synergistic in lung cancer.Journal of carcinogenesis · 2009Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Malignant pleural mesothelioma (MPM) is a disease with few therapeutic options. Protein kinase C beta (PKCbeta) is involved in important cellular functions. Enzastaurin (LY317615.HCl) is a novel inhibitor of PKC in clinical development. MPM cell lines (7) and patient tumor tissues (24) were evaluated for expression of PKCbeta by immunoblotting and immunohistochemistry, respectively. In-vitro cell growth assays were performed with enzastaurin with or without cisplatin. Cell migration was evaluated with the wound healing assay. Downstream signaling (survival and focal adhesion pathways) was studied by immunoblotting for related molecules in the presence of phorbol ester with or without enzastaurin. Expression for PKCbeta1 was seen in all cases, with a mean integrated optical density of 152.5 (standard deviation=95.47, n=24), whereas PKCbeta2 expression was less intense, with a mean integrated optical density of 11.45 (standard deviation=16.27, n=21). There was a trend toward lower overall survival among patients expressing above-median PKCbeta1 (P=0.064), but not PKCbeta2. Robust expression of PKCbeta1 and low expression of PKCbeta2 were observed in MPM cell lines. Treatment of MPM cell lines with enzastaurin revealed an IC50 of 5 micromol/l, and strong synergism was observed when combined with cisplatin. Wound healing assay revealed that treatment of H2461 cells with enzastaurin reduced migration by 59.2%. Enzastaurin treatment led to disruption of F-actin architecture. Downstream signaling showed reduced phosphorylation of AKT, FAK (focal adhesion kinase), p130Cas, S6 ribosomal protein, and paxillin. PKCbeta1 was expressed in the majority of MPM samples. Enzastaurin has preclinical activity against MPM, and exhibited synergism with cisplatin. PKCbeta inhibition in MPM might be able to reduce the invasiveness of MPM by affecting cytoskeletal function.
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